portal hypertensive gastropathy
Introduction
Introduction to portal hypertensive gastropathy In 1985, McCormack et al summarized the special endoscopic and histological features of gastric mucosa in patients with liver cirrhosis, pointing out that the pathological changes of this gastric mucosal lesion are mainly mucosal and submucosal vasodilation, not inflammatory damage, and named congestive. Gastric disease (congestivegastropathy, CG), later changed to portal hypertensive gastropathy (PHG). Most patients in clinical practice have a small amount of hematemesis and melena, which may be associated with anemia. A few cases of upper gastrointestinal bleeding may cause hemorrhagic shock, and may induce hepatic encephalopathy, infection, hepatorenal syndrome and other complications. basic knowledge The proportion of the disease: the incidence of this disease in patients with liver disease is about 0.3% -0.5% Susceptible people: no special people Mode of infection: non-infectious Complications: hypersplenism, ascites, spider mites, upper gastrointestinal bleeding, anemia, hemorrhagic shock, hepatic encephalopathy, hepatorenal syndrome
Cause
Causes of portal hypertensive gastropathy
Mucosal circulatory disorders (30%):
The normal gastric mucosa can concentrate H 1 million times, maintaining a high H concentration gradient between the stomach cavity and the stomach wall. The gastric mucosa relies on abundant blood flow to clear the H entering the stomach wall, and the blood flow force after the portal pressure is increased. Learning changes, submucosal vasodilation, arteriovenous traffic, venous and capillary varices, venous congestion, increased submucosal blood flow, and reduced mucosal blood supply cause ischemia and hypoxia.
Bile reflux (20%):
In portal hypertension, gastrointestinal congestion and hypergastrinemia inhibit the regulation of pyloric sphincter and Oddi sphincter by cholecystokinin and secretin, causing it to relax, and the contents of bile and duodenum flow back into the stomach. Causes bile reflux gastritis.
Impaired liver function (20%):
18.6% of patients with normal or mild liver function developed acute gastric mucosal lesions and hemorrhage, and 55.5% of patients with severe hepatic insufficiency.
Endotoxemia (10%):
Patients with portal hypertension often have endotoxemia, and liver function decompensation is more common, such as 66% to 100% of acute liver failure complicated by endotoxemia; the incidence of hepatic encephalopathy is about 93%; The rate of bleeding was 53.8%.
Infection (5%):
Hepatitis B virus exists in gastric mucosal epithelial cells, which form an antigen-antibody complex and deposit in microvascular endothelial cells, causing an inflammatory reaction and destroying the gastric mucosal barrier.
Stress response (10%):
Critically ill patients, including severe liver patients, often develop stress reactions, resulting in decreased gastrointestinal mucosal blood flow, ischemia and hypoxia and a series of pathophysiological changes.
Prevention
Portal hypertensive gastropathy prevention
Avoid excessive fatigue, it will cause insufficient gastrointestinal blood supply, gastric mucosal secretion disorders, can also lead to a variety of stomach diseases. Stop eating unevenly. Eating and drinking are uneven, the stomach is empty when starving, and the stomach acid and pepsin secreted by the gastric mucosa are a bad stimulus to the stomach wall; overeating also makes the stomach wall over-expand, and the food stays in the stomach for too long, which will be on the stomach. Causes great damage.
Complication
Portal hypertensive gastropathy complications Complications, spleen function, hypertrophic ascites, spider sputum, upper gastrointestinal bleeding, hemorrhagic shock, hepatic encephalopathy, hepatorenal syndrome
Splenomegaly, hypersplenism, hematemesis or melena, ascites or non-specific systemic symptoms (such as fatigue, lethargy, anorexia). Once the varicose esophagus and fundus veins rupture, acute hemorrhage occurs immediately, and red blood is vomited. Hemorrhagic dysfunction caused by liver damage, and thrombocytopenia caused by hypersplenism, so bleeding is not easy to stop. Due to severe hemorrhage caused severe liver hypoxia, it is easy to cause hepatic coma. Other signs of chronic liver disease such as spider mites, liver palm, male breast development, and atrophy of climbing pills may also be present. The clinical manifestations of severe PHG are mainly upper gastrointestinal bleeding. Most of them are a small amount of hematemesis, melena, may be associated with anemia, a small number of upper gastrointestinal bleeding, can cause hemorrhagic shock, and can induce hepatic encephalopathy, infection, liver and kidney syndrome and other complications.
Symptom
Symptoms of portal hypertensive gastropathy Common symptoms Upper gastrointestinal bleeding upper left abdominal mass accompanied by ... Gastroscope showed a wide... Shock hyperemia hepatorenal syndrome
PHG is mostly mild and has no specific clinical symptoms. It is often found during gastroscopy that light PHG can develop into severe PHG over time. The clinical manifestations of severe PHG are mainly upper gastrointestinal bleeding, most of which are small hematemesis and melena. With anemia, a small number of upper gastrointestinal bleeding, can cause hemorrhagic shock, and can induce hepatic encephalopathy, infection, liver and kidney syndrome and other complications, bleeding rate after bleeding is very high.
Examine
Examination of portal hypertensive gastropathy
Patients with cirrhosis often have different degrees of anemia, most of which are normal cell or small cell anemia, occasionally giant cell anemia, erythrocyte formation inhibition may occur in the late stage, whole blood cells decrease in spleen, and promote bleeding, prolong clotting time Prolonged prothrombin time, especially obstructive jaundice, so some patients can be corrected with vitamin K. When acute bleeding, white blood cells increase, return to normal after hemostasis, bleeding is obvious and extensive, should pay attention to DIC, such as decreased platelet count Or progressive reduction, fibrinogen <1 ~ 1.25g / L, FDP> 600mg / L, 3P test positive and euglobulin lysis time shortened, can establish a diagnosis, such as prolonged prothrombin time, euglobulin dissolution time Significantly shortened, and platelet count is normal, 3P test negative, for primary fibrinolysis, blood ammonia may increase after hemorrhage, water and electrolyte disorders and renal dysfunction.
Decompensated cirrhosis, cholesterol ester is lower than normal, albumin is reduced, globulin is increased, white/globulin is inverted, transaminase is slightly elevated, and some cases of post-hepatitis cirrhosis can also detect hepatitis B or hepatitis C virus serum markers. , combined with endotoxemia, sputum test positive.
Endoscopy
The endoscope mainly shows mucosal erythema, and the mucous membrane has a white-yellow fine mesh structure, which divides the red or reddish edema mucosa into a snake-like shape, which is called a snake sign or a mosaic sign. Characteristic manifestations, severely visible in cherry red spots and patchy hemorrhage, endoscopic grading is not yet uniform, McCormack et al. divided PHG endoscopic findings into light and heavy, light manifestations of mucous membranes slightly reddish, streaked Red spot, snake skin sign or mosaic sign, heavy performance is scattered in cherry red spots or diffuse hemorrhagic lesions, Tanoue and other endoscopes are divided into 3 levels: grade I, slight redness, mosaic sign (-); grade II, serious Congestion; Grade III, with grade II flaking on the basis of grade II, this classification method divides the light type in the McCormack classification into two grades, because the boundary between the grades is clear and easy to remember, the literature reports that PHG accounts for half of cirrhosis under endoscopy. Above, mostly light, mosaic signs are the most common.
2. Endoscopic ultrasound
The stomach wall is diffuse and thick, and it is characterized by obvious small vein expansion.
3. Histological characteristics
Submucosal vein dilatation, no or only mild inflammatory cell infiltration is characteristic, other submucosal small arteriovenous wall thickening, venous arterialization, mucosal cross-sectional capillary area is normal, gastric mucosal capillary The vascular dysplasia is scattered in the stomach cavity, the surface is covered with epithelial tissue, the gastric mucosa is straightened, and the helicity is reduced. Small blood vessel injection studies have found that the submucosal arteriovenous shunt is widely open, and electron microscopic observation shows significant expansion of the capillaries. The pores of the endothelium are enlarged, the vascular endothelium is not tightly connected to the basement membrane, the interval is formed, the vascular basement membrane is discontinuous, the distance between the capillary basement membrane and the basement membrane of the epithelial cells is widened, the epithelial cells are swollen and degenerated, and the red blood cells are from the damaged epithelium. Infiltration, and occurs between the epithelial space, because endoscopic biopsy is small and superficial, only 50% of biopsy specimens have telangiectasia.
Diagnosis
Diagnosis and differential diagnosis of portal hypertensive gastropathy
diagnosis
Mainly relying on gastroscope to make diagnosis, cirrhotic patients with portal hypertension showed extensive mucosal erythema under gastroscope, mosaic sign, gastric mucosa, especially at the bottom of the stomach, scattered red spots or multiple red spots and spontaneous bleeding, more can be diagnosed, gastroscope The biopsy was small and superficial. In addition to a certain degree of congestion, there were no obvious abnormalities, which did not help the diagnosis of PHG. It was also reported that 50% of endoscopic biopsy specimens showed telangiectasia.
Differential diagnosis
1. gastric antral vascular ectasias (GAVE)
Under endoscopy, it is characterized by erythema punctate or streaky hemorrhagic erythema, which is more likely to be confused with PHG, but the following points can be used for differential reference: GAVE is not necessarily accompanied by portal hypertension, and endoscopic sinus mucosa More dense point or longitudinal erythema, concentrated from the antrum to the pyloric area, different from PHG mainly manifested as the fundus, the mosaic of the stomach and the scarlet fever rash, compared with PHG, GAVE has obvious gastrointestinal bleeding And anemia, GAVE-related mucosal abnormalities and gastrointestinal bleeding have a good effect on endoscopic electrocoagulation or gastric antrum resection, while PHG requires drug or portal decompression, GAVE under endoscopic antrum The thickness of the stomach wall is less than 1cm, and the mucosa or mucosa is spongy, while the entire stomach wall of PHG is diffuse and thick, with obvious venous dilatation.
2. Other
It is necessary to exclude Helicobacter pylori (Hp)-associated gastritis, alcoholic gastritis, gastric mucosal erosion, drug-related gastritis, biliary gastritis, and gastric vascular dysplasia.
